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anemia/tyrosine

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Bls 1 frá 558 niðurstöður

Oxidative stress-associated protein tyrosine kinases and phosphatases in Fanconi anemia.

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CONCLUSIONS Fanconi anemia (FA) is a genetic disorder featuring chromosomal instability, developmental defects, progressive bone marrow failure, and predisposition to cancer. Besides the predominant role in DNA damage response and/or repair, many studies have linked FA proteins to oxidative stress.
OBJECTIVE To observe the clinical effect of Busui Shengxue Granule (BSG) in treating chronic aplastic anemia (CAA) and the changes of serum fibronectin (Fn) level and expression of FMS-like tyrosine kinase 3 ligand (FL). METHODS Sixty-eight patients with CAA were assigned to two groups. The 35

T-cell expression of Bruton's tyrosine kinase promotes autoreactive T-cell activation and exacerbates aplastic anemia.

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The role of Bruton's tyrosine kinase (BTK) in BCR signaling is well defined, and BTK is involved in B-cell development, differentiation, and malignancies. However, the expression of Btk in T cells and its role in T-cell function remain largely unknown. Here, we unexpectedly found high expression and
The molecular mechanism of anemia that is hyporesponsive to recombinant human erythropoietin (rHuEPO) in hemodialysis patients without underlying causative factors has not been investigated fully in hematopoietic stem cell system. Circulating CD34+ cells (1 x 10(4)) were isolated from rHuEPO

Tyrosine kinase inhibitor use in pediatric Philadelphia chromosome-positive acute lymphoblastic anemia.

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Until recently, pediatric Philadelphia chromosome-positive (Ph(+)) acute lymphoblastic leukemia (ALL) was associated with an extremely poor outcome when treated with chemotherapy alone, and only modest survival benefits were obtained with the widespread use of hematopoietic stem cell transplantation
Ten patients with manifest iron deficiency and without documented relationship to phenylketonuria patients were orally loaded with 25 mg/kg of L-(2H5)phenylalanine. Before loading, the fasting phenylalanine-tyrosine plasma ratio was determined and after loading, the concentrations of labeled and

Mechanisms of anemia in SHP-1 protein tyrosine phosphatase-deficient "viable motheaten" mice.

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OBJECTIVE Viable motheaten mice (abbreviated gene symbol me(v)) are deficient in SHP-1, a critical negative regulator of signal transduction in hematopoietic cells. These mice exhibit severe immune dysfunction accompanied by hyperproliferation of myeloid cells, widespread inflammatory lesions, and

Mutation of chicken anemia virus VP2 differentially affects serine/threonine and tyrosine protein phosphatase activities.

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Novel dual-specificity protein phosphatases (DSPs), which catalyse the removal of phosphate from both phosphotyrosine and phosphoserine/phosphothreonine substrates, have recently been identified in two viruses within the family Circoviridae. Viral protein 2 (VP2) of chicken anemia virus (CAV) and

[Urinary tyrosine in pernicious anemia and leukemia in comparison with normal conditions].

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Metabolism of tyrosine in experimental megaloblastic anemia and in scurvy in the monkey.

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Antipernicious anemia extracts and tyrosine metabolism in the scorbutic guinea pig.

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A child of Italian origin with a congenital haemolytic anaemia had spectrophotometrically undetectable erythrocyte adenylate kinase (AK) activity. Her parents and brother had approximately 50% normal AK activity, and AK electrophoresis of red blood cell (RBC) crude extract on cellulose acetate

Chicken anemia virus VP2 is a novel dual specificity protein phosphatase.

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The function of viral protein 2 (VP2) of the immunosuppressive circovirus chicken anemia virus (CAV) has not yet been established. We show that the CAV VP2 amino acid sequence has some similarity to a number of eukaryotic, receptor, protein-tyrosine phosphatase (PTPase) alpha proteins as well as to
Fanconi anemia (FA) is an autosomal recessive disorder with a high risk of malignancies including acute myeloid leukemia and squamous cell carcinoma. There is a constant search out of new potential therapeutic molecule to combat this disorder. In most cases, patients with FA develop haematological
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